The target organ of submersion injury is the lung. Injury to other systems is largely secondary to hypoxia and ischemic acidosis. Additional CNS insult may result from concomitant head or spinal cord injury. Fluid aspirated into the lungs produces vagally mediated pulmonary vasoconstriction and hypertension. Fresh water moves rapidly across the alveolar-capillary membrane into the microcirculation. Surfactant is destroyed, producing alveolar instability, atelectasis, and decreased compliance with marked ventilation/perfusion (V/Q) mismatching. As much as 75% of blood flow may circulate through hypoventilated lungs. In salt water near drowning, surfactant washout occurs, and protein-rich fluid exudates rapidly into the alveoli and pulmonary interstitium. Compliance is reduced, alveolar-capillary basement membrane is damaged directly, and shunting occurs. This results in rapid induction of serious hypoxia. Fluid-induced bronchospasm also may contribute to hypoxia.
In a minor percentage of patients, aspiration of vomitus, sand, silt, and sewage may result in occlusion of bronchi, bronchospasm, pneumonia, abscess formation, and inflammatory damage to alveolar capillary membranes. Postobstructive pulmonary edema following laryngeal spasm and hypoxic neuronal injury with resultant neurogenic pulmonary edema also may play roles.
In short, significant cellular tissue damage also occurs and would be present and detectable even if the water wasn't. There was no evidence of drowning in Danielle's lungs.